TCF/beta-catenin plays an important role in HCCR-1 oncogene expression
DC Field | Value | Language |
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dc.contributor.author | Cho, Goang-Won | - |
dc.contributor.author | Kim, Mi-Hwa | - |
dc.contributor.author | Kim, Seung Hyun | - |
dc.contributor.author | Ha, Seon-Ah | - |
dc.contributor.author | Kim, Hyun Kee | - |
dc.contributor.author | Kim, Sanghee | - |
dc.contributor.author | Kim, Jin W. | - |
dc.date.accessioned | 2022-12-20T22:27:19Z | - |
dc.date.available | 2022-12-20T22:27:19Z | - |
dc.date.created | 2022-08-26 | - |
dc.date.issued | 2009-05 | - |
dc.identifier.issn | 1471-2199 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/176873 | - |
dc.description.abstract | Background: Oncogene HCCR-1 functions as a negative regulator of the p53 and contributes to tumorigenesis of various human tissues. However, it is unknown how HCCR-1 contributes to the cellular and biochemical mechanisms of human tumorigenesis. Results: In this study, we showed how the expression of HCCR-1 is modulated. The luciferase activity assay indicated that the HCCR-1 5'-flanking region at positions -166 to +30 plays an important role in HCCR-1 promoter activity. Computational analysis of this region identified two consensus sequences for the T-cell factor (TCF) located at -26 to -4 (Tcf1) and -136 to -114 (Tcf2). Mutation at the Tcf1 site led to a dramatic decrease in promoter activity. Mobility shift assays (EMSA) revealed that nuclear proteins bind to the Tcf1 site, but not to the Tcf2 site. LiCl, Wnt signal activator by GSK-3 beta inhibition, significantly increased reporter activities in wild-type Tcf1-containing constructs, but were without effect in mutant Tcf1-containing constructs in HEK/293 cells. In addition, endogenous HCCR-1 expression was also increased by treatment with GSK-3 beta inhibitor, LiCl or AR-A014418 in HEK/293 and K562 cells. Finally, we also observed that the transcription factor, TCF, and its cofactor, beta-catenin, bound to the Tcf1 site. Conclusion: These findings suggest that the Tcf1 site on the HCCR-1 promoter is a major element regulating HCCR-1 expression and abnormal stimulation of this site may induce various human cancers. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | BMC | - |
dc.title | TCF/beta-catenin plays an important role in HCCR-1 oncogene expression | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Seung Hyun | - |
dc.identifier.doi | 10.1186/1471-2199-10-42 | - |
dc.identifier.scopusid | 2-s2.0-67649419563 | - |
dc.identifier.wosid | 000266807000002 | - |
dc.identifier.bibliographicCitation | BMC MOLECULAR BIOLOGY, v.10, pp.1 - 9 | - |
dc.relation.isPartOf | BMC MOLECULAR BIOLOGY | - |
dc.citation.title | BMC MOLECULAR BIOLOGY | - |
dc.citation.volume | 10 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 9 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | COLORECTAL-CANCER | - |
dc.subject.keywordPlus | BETA-CATENIN | - |
dc.subject.keywordPlus | COLON-CANCER | - |
dc.subject.keywordPlus | WNT | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | POLARITY | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.identifier.url | https://bmcmolbiol.biomedcentral.com/articles/10.1186/1471-2199-10-42 | - |
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